抄録
Effects of aconitine and veratridine on membrane currents in the crayfish giant axon were studied under voltage-clamped conditions. Aconitine at 50μM reduced the Na current without changing the K current. The Na current left after aconitine block showed the activation and inactivation kinetics unaltered from the normal. These aconitineeffects differ from those reported previously with myelinated nerves. The rate of Na channel block by aconitine was increased with increasing either frequency or voltage of depolarizing pulses delivered repetitively from the holding potential but was not affected by a change in the pulseduration from 2 to 10msec. The same change in the pulse duration, however, caused about a 4-fold increase in the blocking rate in the axon of which inactivation process had been removed by a pretreatment with a sea anemone toxin from Parasicyonis actinostoloides. These results are explained by a model in which Na channels are occluded with aconitine molecules only when the channels are open. Veratridine at 50μM also exhibited frequency-dependent actions, depressing the maximum peak inward current and shifting the reversal potential of the transient current in the hyperpolarized direction. These veratridine effects persisted after washing. In addition to such persistent actions, veratridin induced a maintained Na current at the holding potential during repetitive stimulation. This effect was abolished after a brief wash unlike the above-mentioned persistent effects, suggesting that veratridine has two (or more) different modes of actions on Na channels in the crayfish giant axon.
